| Discussion: |
The main raison d'etre of parathormone is to increase the level of serum ionized calcium. To do this, it acts on the gut, kidney, and bones. In the gut, it increases the absorption of dietary calcium. In the kidneys, phosphate resorption is decreased, causing elevation of the calcium level. Parathormone causes resorption of calcium from the bones, which act as a giant calcium warehouse.
Therefore, the main finding in the bones with hyperparathyroidism is osteopenia of various types. This may present as a diffuse global osteopenia, or one may see more focal evidence of bone resorption. Some of this resorption occurs in nonspecific patterns, such as intracortical tunneling, endosteal resorption, or trabecular resorption, which can all be seen in many other causes of osteopenia. However, hyperparathyroidism can also present with more specific patterns of osteopenia, such as that seen in the skull above, or in the fingers below in the same patient.
Views of the left index finger in the same patient show typical finger findings of hyperparathyroidism, with bone resorption from the distal tuft and subperiosteal areas. Such subperiosteal resorption is virtually pathognomonic for hyperparathyroidism, and usually more common along the radial margin of the fingers, for reasons which are obscure. After successful treatment of the cause of hyperparathyroidism (e.g. resection of an adenoma), the bone resorption may reverse, as shown above.
Osteopenia may result from many causes. It may be helpful to first decide if a patient's osteopenia is generalized or regional (limited to a particular part of the body).
Since the finger films were craftily withheld from your initial consideration, it was not possible for your to tell whether this patient had a generalized or more localized process. The addition of the finger films makes it clear that this is, indeed, a generalized process, and also adds findings that are even more specific for hyperparathyroidism.
If one considers the skull findings alone, many of the entities in the differential tables above could have caused lucent skull lesions. However, the diffuse pattern of punctate lucencies shown is characteristic of the classic "salt and pepper" appearance seen in hyperparathyroidism. The complete regression of the findings following treatment is also strongly suggestive of hyperparathyroidism. Multiple myeloma, for example, can cause multiple lytic lesions of the skull, but they tend to be larger and more sharply defined. Also, the complete disappearance of lesions following treatment would be unusual for myeloma or other malignancies. Various anemic states can affect the skull, but are likely to cause widening of the diploic space. Paget's disease can cause lytic lesions of the skull, but these tend to be larger and more geographic in appearance. Once the lytic phase of Paget's disease has passed, sclerosis and bony enlargement usually follows, rather than a return to normal-appearing bone.